RAD-140 (Testolone): A Complete SARM Guide

RAD-140, commonly referred to as Testolone, is a non-steroidal selective androgen receptor modulator (SARM) originally developed by Radius Health as an investigational agent for conditions associated with muscle wasting and, later, hormone-sensitive breast cancer. Among the SARM class it is frequently described in the literature as having one of the higher anabolic-to-androgenic activity ratios, and for that reason it occupies a specific position in how researchers stage SARM protocols. This reference piece summarizes the binding profile, the dosing range reported in human and preclinical work, observed suppression, post-cycle considerations, hepatic signals, and how RAD-140 compares with LGD-4033 within a progression framework.

Binding profile and mechanism

RAD-140 is a small-molecule, non-steroidal ligand of the androgen receptor (AR). Unlike testosterone and 17-alpha-alkylated oral anabolics, it does not share the steroid backbone, and its interaction with the AR is tissue-selective — binding preferentially produces transcriptional effects in muscle and bone while showing relatively lower activity at the prostate, skin, and hair follicle. This selectivity is the defining pharmacological feature researchers reference when distinguishing SARMs from traditional androgens.

In the early in vitro and rodent work published by Miller and colleagues in 2011, RAD-140 demonstrated high AR binding affinity and a favorable anabolic index in myotrophic-versus-androgenic assays, with anabolic:androgenic ratios frequently cited in the 90:1 range under the specific assay conditions used. These numbers are assay-dependent and do not translate linearly to human outcomes, but they are consistent with the general pattern of strong skeletal-muscle AR engagement at doses that produce comparatively modest prostate effects in the animal models.

A point often understated in secondary sources: RAD-140 has also been investigated as a partial agonist in AR-positive breast cancer cell lines. Work by Yu and colleagues reported activity against tamoxifen-resistant cell lines, which is why Radius Health advanced the compound into oncology trials under the code RAD1901/RAD140. For the purposes of this guide, that context matters because it is the source of most human pharmacokinetic data available — oncology-dose exposure, not performance-dose exposure.

Dosing literature

Human dosing information for RAD-140 is limited and almost entirely derived from the Phase 1 oncology program, where doses were escalated in cancer patients rather than healthy volunteers. In that setting, daily oral doses in the range of tens of milligrams were administered, with adverse event reporting that included transaminase elevations at higher dose levels. Researchers should note that oncology populations are not directly comparable to non-clinical research contexts.

Within the grey literature and the harm-reduction discussions that surround SARMs, the commonly referenced range is 10 to 20 mg per day taken orally, typically as a single dose given the reported half-life of roughly 20 hours in early pharmacokinetic work. Protocols at the lower end (10 mg) are often described in first-exposure contexts, with the upper end (20 mg) reserved for subjects with prior SARM exposure. Doses above 20 mg are not well-characterized in any accessible dataset and are associated with a steeper rise in reported side effects without a clearly documented proportional increase in lean mass outcomes.

Cycle length in reported protocols clusters around 8 weeks. Shorter cycles of 6 weeks are also common. Extensions beyond 8 weeks are rarely described in the literature and are associated with increased suppression and a longer recovery window. A representative protocol framework used in reference discussions:

• Weeks 1–8: 10–20 mg RAD-140 once daily, oral
• Weeks 9–12: post-cycle therapy (see below)
• Minimum off-cycle: equivalent to the length of the cycle plus PCT before any subsequent exposure

These are reference ranges drawn from reported protocols, not prescriptive recommendations. The compound is not approved for human use outside of clinical trials.

Suppression of endogenous androgens

Suppression of the hypothalamic-pituitary-gonadal (HPG) axis is the most consistently reported endocrine finding across SARM user-reported data and the limited clinical literature. Within the SARM class, RAD-140 is characterized as a strong suppressor — frequently ranked alongside or above LGD-4033 in subjective reports and in the small amount of hormonal data available from self-reported bloodwork databases.

In practical terms, subjects on 10–20 mg RAD-140 for 8 weeks commonly report total testosterone dropping into the low or sub-reference range by mid-cycle, with LH and FSH also suppressed. The mechanism is the same as for exogenous androgens: AR-mediated negative feedback at the hypothalamus and pituitary reduces gonadotropin output, which in turn reduces testicular testosterone production. Because RAD-140 is not aromatized in the same way as testosterone, estradiol typically falls along with testosterone rather than rising, which produces its own symptom profile — lower libido, flatter mood, reduced recovery — distinct from the high-estrogen picture seen with traditional anabolics.

Recovery timelines in reported post-cycle bloodwork are variable. Some subjects show return to baseline LH and testosterone within 4 to 6 weeks of discontinuation with a SERM-based PCT; others show prolonged suppression extending beyond 8 weeks, particularly after longer cycles or stacked protocols. Baseline hormonal panels before initiation, a mid-cycle panel, and a post-PCT panel are the minimum monitoring set referenced in harm-reduction discussions.

Post-cycle therapy

Because suppression is expected rather than incidental, a structured post-cycle therapy (PCT) protocol is standard in reported RAD-140 use. The most common SERM referenced is tamoxifen (Nolvadex), which blocks estrogen receptors at the hypothalamus and pituitary, disinhibiting gonadotropin release and accelerating the return of endogenous testosterone production.

A representative PCT structure referenced alongside an 8-week RAD-140 cycle:

• Weeks 1–2 post-cycle: Nolvadex 20 mg/day
• Weeks 3–4 post-cycle: Nolvadex 10 mg/day

Clomiphene (Clomid) is sometimes substituted or combined, though Nolvadex alone is the more common single-agent approach for a SARM-only cycle of this length. Enclomiphene is occasionally discussed as a cleaner alternative given its reduced estrogenic activity relative to clomiphene, but human data in the PCT context is limited.

Researchers should note two points. First, SERMs themselves carry a side-effect profile — visual disturbances with clomiphene are well-documented, and Nolvadex carries a small but real thromboembolic signal in the oncology literature. Second, a bloodwork-confirmed return to baseline is more informative than a fixed calendar window; if LH and testosterone remain suppressed at the 4-week post-PCT panel, extension is sometimes warranted rather than initiating a second cycle.

Hepatotoxicity and monitoring

RAD-140 is not a 17-alpha-alkylated oral and does not share the hepatotoxicity profile of compounds like methandrostenolone or oxymetholone, where the alkyl modification is itself the primary driver of liver strain. That said, transaminase elevations have been reported in both the oncology trial data and in user-reported bloodwork, and the compound should not be treated as hepatically inert.

The pattern that appears in reported bloodwork is a mild-to-moderate rise in AST and ALT during the cycle, typically resolving within weeks of discontinuation. The magnitude is generally smaller than what is seen with 17aa orals at performance-range doses, but it is non-trivial, and it is dose-dependent. A 2020 case report by Barbara and colleagues described a case of drug-induced liver injury associated with RAD-140 use, underscoring that idiosyncratic hepatic reactions are possible even at protocol-typical doses.

Monitoring recommendations drawn from reported practice:

• Baseline comprehensive metabolic panel including AST, ALT, GGT, bilirubin
• Mid-cycle repeat at week 4
• Post-cycle repeat 4–6 weeks after discontinuation
• Avoid concurrent hepatotoxic agents — alcohol, high-dose NSAIDs, other 17aa compounds

Lipid changes are a separate and consistent finding. HDL reductions are reported across the SARM class and have been documented with RAD-140; LDL shifts are more variable. A full lipid panel belongs in the same monitoring schedule as the liver markers.

Position in a SARMs progression

Within a staged SARMs framework, RAD-140 is not usually the first exposure. The commonly referenced progression places milder, better-characterized compounds earlier — ostarine (MK-2866) at 10–20 mg for a first cycle, then LGD-4033 at 5–10 mg as a second-step compound — before moving to RAD-140.

The comparison with LGD-4033 is the most useful reference point. LGD-4033 is generally reported as producing comparable or slightly greater lean-mass changes at lower absolute doses (5–10 mg versus 10–20 mg), with a similar suppression profile and a somewhat better-characterized human safety dataset from its Ligand Pharmaceuticals Phase 1 program. RAD-140 is often described as producing a "drier", more androgenic subjective profile — more aggression, more strength expression, less water retention — though these descriptors come from user-reported data rather than controlled comparison trials.

Stacking RAD-140 with other SARMs is discussed in the reported literature but compounds the suppression and hepatic-lipid burden without a corresponding dataset to support the risk-benefit tradeoff. Single-compound cycles with full monitoring and a structured PCT are the baseline reference pattern; stacked protocols move further from the characterized evidence base.

A short summary of where RAD-140 sits:

• Stronger suppression than ostarine, comparable to or slightly above LGD-4033
• Higher subjective androgenic expression than LGD-4033
• Mandatory SERM-based PCT, not optional
• Hepatic and lipid monitoring warranted, more so than for ostarine
• Not a first-cycle compound in most reported progression frameworks

Open questions

The RAD-140 evidence base has visible gaps that researchers should hold in mind when interpreting protocol recommendations. Long-term human exposure data outside the oncology trial population is essentially absent — the compound has been in grey-market circulation for roughly a decade, but there is no prospective cohort tracking cardiovascular, hepatic, or endocrine outcomes in non-clinical users. The true incidence of idiosyncratic liver injury at protocol-typical doses is unknown.

Recovery heterogeneity is another open area. Why some subjects return to baseline HPG function within 6 weeks post-PCT and others remain suppressed at 12 weeks is not explained by the currently available data, and no reliable pre-cycle predictor of slow recovery has been validated. The interaction between repeated cycles and cumulative suppression risk is similarly uncharacterized.

Finally, the oncology development program for RAD-140 was discontinued, which means the most rigorous source of human pharmacokinetic and safety data has stopped expanding. Any additional clarity on dose-response, exposure-toxicity relationships, or long-term signals will have to come from observational work on non-clinical use — a dataset that is difficult to build and, at present, fragmentary.